This research program is involved with studies of the response of vessel walls to injury. Functional and growth properties and response to injuries of endothelium, intimal and medial smooth muscle and myocardial cells are being investigated in vivo and in vitro by means of ultrastructural, chemical, and cell culture analysis. The chemical structure and production of basement membrane in vessels and its role in repair of myocardial cells after local cardiac injury are being investigated. Source and functions of amyloid protein AA is under investigation. The properties and origins of the cells of the atherosclerotic plaques of humans are being investigated. A new way of viewing risk factors in atherosclerosis is being explored. The presence of mutagens derived from the environment (e.g., cigarette smoke) or from endogenous cholesterol in human lipoproteins is being looked for. Mast cell interactions with lipids and lipoproteins and the relationship to heparin are being studied. The role of mixed function oxygenases in metabolism of promutagens to mutagens or cytotoxic agents by artery wall is being investigated. The possible ways by which mutagens (extrinsic or intrinsic) may induce the cell population of atherosclerotic plaques to be monoclonal is under investigation. How hypertension and its chemical mediators affect the artery wall and may augment rates of atherosclerosis are being investigated.